On the other hand, in obese mice that showed vasoconstrictor response and endothelial dysfunction, mineralocorticoid receptor antagonist (MRA) treatment led to reduced expression of pro-oxidative NADPH oxidase and increased levels of the antioxidative enzymes glutathione peroxidase-1 and superoxide dismutase-1 and -3 in endothelial cells, with potential protection against endothelial alterations [5], suggesting that MRA administration may represent a valid therapeutic strategy to counteract vascular dysfunction and atherosclerotic complications induced by MR overactivation. The gene discussed is NR3C2; the disease is endothelial dysfunction.